The electronic cigarette or e-cigarette is the new alternative method to deliver nicotine. In 2007, the United States introduced vaping devices on the market. Due to their attractive taste and lack of adverse effects, these vaping devices have gained popularity among youth and adults. However, there has been increasing evidence that vaping can cause severe lung injury, and these devices release toxic chemicals into the body. E-cigarettes are recognized as a global threat to public health. Nicotine, the most prevalent chemical in vaping devices, is associated with neurological problems and cognitive decline. Long-term use of e-cigarettes can cause adverse health problems, including respiratory illnesses, asthma, bronchitis, and lung inflammation. In 2019, the Centers for Disease Control and Prevention (CDC) officially declared vaping-associated illness EVALI (e-cigarette or Vaping Product Associated Lung Injury). The US Surgeon General published an alarm in December 2016 that e-cigarette consumption among adolescents and teens in the US is a “major public health concern” and that more young people are now vaping than smoking traditional cigarettes and cigars. Since its commercial introduction in 2003, modern electronic cigarettes (or E-cigarette s) have become increasingly popular with smokers, non-smokers, and those who used to smoke who have switched to them. With such a rise in consumption, people are becoming more aware of the irritating, harmful, and perhaps cancer-causing effects on the lungs.

Parkinson’s Disease (PD) is a serious neurodegenerative disease, especially in the elderly population, with a very high incidence and no effective clinical treatment. Ramelteon is a melatonin receptor agonist that can be used to treat sleep-resistant insomnia, and it also has a definite effect on chronic insomnia and short-term insomnia, and is the first non-addictive insomnia treatment drug that is not listed as a special control. Ramelteon has been shown to alleviate inflammation and oxidative stress by activating the Nrf2 signaling pathway, thereby preventing traumatic brain injury. Ramelteon has also been shown to delay cell senescence in the Parkinson’s model of human SH-SY5Y neuronal cells, however, no studies have shown whether Ramelteon can alleviate Parkinson’s by inhibiting neuroinflammation. To this end, this study investigated whether Ramelteon can achieve a neuroprotective effect on 6-OHDA-treated human SH-SY5Y neuronal cells and Parkinson’s mouse models through the NF-κB pathway. In this study, we found that Ramelteon could potently inhibit ROS release from 6-OHDA-treated SH-SY5Y neuronal cells, improve dyskinesia in Parkinson’s mouse models, and effectively inhibit neuroinflammation via the NF-κB pathway. In conclusion, Ramelteon can inhibit neuroinflammation through the NF-κB pathway, thereby achieving neuroprotective effects on Parkinson’s mouse models.

Background : MicroRNAs (miRNAs) play key regulatory roles as oncogenes or anti-oncogenes at the posttranscriptional level in human cancers. Plant miRNAs can regulate mammalian systems across kingdoms. The present study investigated the effects of plant miRNA157 (miR157) on the viability and proliferation of human hepatoma cells and the underlying mechanisms.

Method : The potential targets of miR157 were predicted by bioinformatics methods; the targeted regulatory relationship between miR157 and MTDH was detected by dual luciferase reporter assay; hepatoma cells HepG2 were cultured in vitro and divided into control group (transfected with negative control SNC mimics) and miR157 transfection group (transfected with miR157 mimics). After transfection, cell counting kit-8 and colony formation were used to detect cell proliferation ability, and RT-qPCR and Western blot were used to detect the effect of miR157 on MTDH expression in HepG2 cells

Results: miR157 had an inhibitory effect on the proliferative capacity of hepatoma cells HepG2 (P<0.05); dual-luciferase reporter gene assay showed that MTDH is a target gene of miR157; miR157 could be directly targeted to down-regulate the expression of MTDH (P<0.01).

Conclusion : These preliminary pieces of evidence suggest that miR157 inhibits the proliferation of HepG2 cells by targeting MTDH.